The overall objective of this work is to understand the photobiological mechanisms involved in chronic environmental UV damage to mammalian skin in a manner sufficient to accurately explain and predict the photobiological consequences of on-going ozone depletion on chronic epidermal and dermal damage, including photocarcinogenesis and "photoaging." Observed action spectra are dose- and time-dependent ("dynamic"), mainly due to UV-induced hyperplasia. Correction for this effect allows construction of "intrinsic" action spectra that can be convoluted with various solar spectral distributions (including those which simulate changes due to stratospheric ozone depletion) to afford "biologically effective doses" under the various atmospheric conditions. Specifically, we wish to (l) expand ongoing photobiological studies in Sk-1 hairless mice to include clinical, histological, and biochemical responses as a function of total dose, wavelength, and dose delivery. We will monitor UV-induced increases in pyrimidine dimers, acid glycosminoglycans (GAG), and changes in collagen structure and fluorescence properties. (2) Construct action spectra for UV-induced DNA and dermal damages. These will be "corrected" for non-uniform absorption of incident radiation by inert stratum corneum-epidermis, to afford "intrinsic" action spectra. (3) Compare the effect of broad- vs. narrow band radiation on the dose-response and action spectra obtained above (test for UVA/UVB waveband interactions). In addition to providing fundamental photochemical and biochemical information, the mechanistic insight provided by these studies should enable more accurate explanation and prediction of photobiological consequences of ozone depletion or other atmospheric changes which would alter the amount of solar UV in the environment.